Inflammatory angiogenesis in atherogenesis--a double-edged sword

Area of Science:

• Cardiovascular Biology
• Vascular Biology
• Pathophysiology

Background:

• Atherosclerosis involves the buildup of plaques in artery walls.
• Vasa vasorum vascularize the outer arterial wall and can sprout into atherosclerotic lesions.
• A proangiogenic microenvironment within lesions drives neovascularization.

Purpose of the Study:

• To explore the role of angiogenesis in atherosclerosis progression.
• To understand the balance of angiogenic factors in atherosclerotic plaques.
• To evaluate the potential of targeting angiogenesis for therapeutic intervention.

Main Methods:

• Analysis of angiogenic and antiangiogenic factors within atherosclerotic lesions.
• Investigation of the impact of neovascularization on plaque growth and stability.
• Review of animal models and clinical study considerations for angiogenesis inhibition.

Main Results:

• Neovascularization is driven by hypoxia, oxidant stress, and inflammatory cells (macrophages, T cells, mast cells).
• An imbalance favoring angiogenic inducers promotes neovessel development.
• Neovascularization initially stabilizes plaques but can lead to rupture via intraplaque hemorrhage.

Conclusions:

• Angiogenesis has a complex, stage-dependent role in atherosclerosis.
• Further research is needed to clarify the net effect of angiogenesis in lesion development.
• Clinical strategies targeting angiogenesis require a comprehensive understanding of its dual role.